The ECG sign of subendocardial ischemia is ST segment depression (A). Depression is reversible if ischemia is only transient but depression persists if ischemia is severe enough to produce infarction. T wave inversion with or without ST segment depression (B) is sometimes seen but not ST segment elevation or Q wave. That is why subendocardial infarction is also called non-ST-elevation myocardial infarction (NSTEMI) and less commonly non-Q wave myocardial infarction.

ST segment depression seen in subendocardial ischemia or infarction can take on different patterns: The most typical being horizontal or down-sloping depression.Up-sloping ST depressionis less specific. In exercise stress tests, horizontal or down-sloping depression of 1 mm or more (A, B, & C) or up-sloping depression of the same magnitude 80 ms beyond the J point (D) is considered positive signs of ischemia. Up-sloping depression of less than 1 mm at 80 ms beyond the J point (E) is simply J point depression and not ST segment depression.

In transmural MI, ischemia in the subendocardium spreads to the epicardium and involves full thickness of the myocardium. In the acute phase, the ECG signs are ST segment elevation.

The elevated ST segment may slope upward or be horizontal or dome-shape.

Hyperacute (tall positive) T waves may precede ST segment elevation (A) or seen at the same time with ST elevation (B) during this acute phase.

Hours to days later during the evolving phase, pathological Q waves appear, the elevated ST segments return towards baseline, and the T waves become inverted.

Q wave is normal if it is shallow and brief (A).

Q wave is pathological if it is wider than 40 ms or deeper than a third of the height of the entire QRS complex (B & C). Significant Q wave usually persists even after recovery.

Localization of myocardial infarction

By way of their position, the 12 ECG leads can be used to distinguish myocardial infarction occurring in different regions of the heart. The chest leads cluster around the heart in the horizontal plane and look in from the front (V1 to V4) and from the left (V5 and V6); leads I and aVL also look in from the left whileleads II, III, and aVF look in at the under surface.

Signs of anterior MI (grey area), territory supplied by the left anterior descending coronary artery (LAD), are seen in V1 to V4.

Signs of lateral MI (grey area), territory supplied by the left circumflex coronary artery (LC), are seen in leads I, aVL, V5 and V6.

Signs of inferior MI (grey area), territory supplied by the right coronary artery (RCA), are seen in leads II, III, and aVF.

Signs of posterior MIon a 12-lead ECG are not the characteristic ST elevation and Q waves, which would be the case if there is a lead recording from the patientíŽs back. Since V1 and V2 are attached to the patientíŽs front, they will record changes reciprocal to changes seen from the back, which are ST depression and tall R waves. These uncharacteristic signs make the diagnosis of posterior MI difficult without heightened vigilance. Suffice it to say, pure posterior wall infarctions are rare. Most extend to involve the inferior wall or lateral wall and leads II, III, and aVF should be examined for characteristic signs of this extension in the former and leads I, aVL, V5 and V6 in the latter.

MI in the presence of LBBB

The presence of LBBB complicates the ECG diagnosis of acute MI. This is because LBBB alone can produce signs that may be confused with those of infarction: deep QS waves in the right chest leads and ST depression and T wave inversion in the left chest leads. Furthermore, the Q wave of left ventricular MI may be buried within the widened QRS complex. Therefore, the diagnosis of acute myocardial infarction should be made circumspectively in the presence of pre-existing LBBB. On the other hand, the appearance of new LBBB should be regarded as sign of acute MI until proven otherwise.